Trigeminal neuralgia is usually caused by demyelination resulting from vascular compression of trigeminal sensory fibers within either the nerve root or the brainstem. Other causes where demyelination is involved or implicated include multiple sclerosis, compressive space occupying masses in the posterior fossa. These focal demyelination areas have close apposition of demyelinated axons and an absence of intervening glial processes. It is this anatomical arrangement that coupled with pulsatile vascular indentation which favors the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibers, and increased spontaneous nerve activity. Decompression results in separation of demyelinated axons and their release from focal distortion leading to rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia. Anticonvulsants, such as carbamazepine, phenytoin, gabapentin, lamotrigine, oxcarbazepine, and topiramate are the mainstay of pharmacotherapy of this condition. These medications are initially effective for pain control in 90% patients. When the patients become refractory to the pharmacotherapy surgical interventions are warranted. On the basis of clinical studies microvascular decompression seem to be the most effective treatment in terms of patient satisfaction and cost effectiveness. The peripheral procedures have higher recurrence rate and complications and have relatively lower long term cost effectiveness